INT137767

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Context Info
Confidence 0.34
First Reported 2005
Last Reported 2011
Negated 5
Speculated 1
Reported most in Body
Documents 74
Total Number 81
Disease Relevance 89.32
Pain Relevance 20.48

This is a graph with borders and nodes. Maybe there is an Imagemap used so the nodes may be linking to some Pages.

Anatomy Link Frequency
spinal cord 13
microglia 4
T cells 4
brain 3
plasma 2
Eae1 (Mus musculus)
Pain Link Frequency Relevance Heat
Multiple sclerosis 2264 100.00 Very High Very High Very High
Central nervous system 1589 100.00 Very High Very High Very High
Spinal cord 867 99.98 Very High Very High Very High
chemokine 693 99.98 Very High Very High Very High
cytokine 644 99.98 Very High Very High Very High
Inflammation 2038 99.96 Very High Very High Very High
Neuritis 125 99.90 Very High Very High Very High
Inflammatory mediators 48 99.56 Very High Very High Very High
antagonist 88 99.42 Very High Very High Very High
COX2 91 99.40 Very High Very High Very High
Disease Link Frequency Relevance Heat
Multiple Sclerosis 6961 100.00 Very High Very High Very High
Stress 1205 100.00 Very High Very High Very High
Syndrome 48 100.00 Very High Very High Very High
Thyroiditis 28 100.00 Very High Very High Very High
INFLAMMATION 2164 99.96 Very High Very High Very High
Optic Neuritis 122 99.90 Very High Very High Very High
Disease 1850 99.80 Very High Very High Very High
Brain Hemorrhage 3 99.68 Very High Very High Very High
Sprains And Strains 297 99.64 Very High Very High Very High
Autoimmune Disease 488 99.28 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Naltrexone, an opioid antagonist, has been shown to modulate expression of experimental autoimmune encephalomyelitis (EAE), an animal model of MS, suggesting that endogenous opioids are inhibitory trophic factors in EAE.
Gene_expression (expression) of EAE associated with multiple sclerosis, antagonist, endogenous opioid and opioid
1) Confidence 0.34 Published 2010 Journal Brain Res. Section Abstract Doc Link 19931226 Disease Relevance 0.68 Pain Relevance 0.58
To confirm this we first measured conduction velocity of EAE callosal axons in the absence and presence of oestrogen receptor ?
Gene_expression (axons) of EAE associated with multiple sclerosis
2) Confidence 0.27 Published 2010 Journal Brain Section Body Doc Link PMC2947430 Disease Relevance 0.53 Pain Relevance 0.25
Scatter plots of axon diameter versus g ratio (iii) and axon diameter versus myelin thickness (iv) indicated demyelination-induced decreases in myelin thickness in vehicle-treated EAE callosal axons, whereas oestrogen receptor ?
Gene_expression (axons) of EAE associated with multiple sclerosis and demyelination
3) Confidence 0.27 Published 2010 Journal Brain Section Body Doc Link PMC2947430 Disease Relevance 1.13 Pain Relevance 0.09
Axonal injury was a severe and acute event, insofar as serum pNF-H levels were not significantly elevated at early (EAE day 12) or late (EAE days 35 and 50) disease time points.
Gene_expression (day) of EAE associated with multiple sclerosis, injury and disease
4) Confidence 0.24 Published 2008 Journal J. Neurosci. Res. Section Abstract Doc Link 18709652 Disease Relevance 1.95 Pain Relevance 0.29
Histopathological evaluation of the brain, cerebellum and spinal cord was performed in WT and B2-/- mice at day 14 after EAE induction.
Gene_expression (induction) of EAE in spinal cord associated with multiple sclerosis and spinal cord
5) Confidence 0.23 Published 2008 Journal J Neuroinflammation Section Body Doc Link PMC2596102 Disease Relevance 1.14 Pain Relevance 0.28
In addition, histopathological analysis of spinal cord for EAE WT mice showed a marked inflammatory response with intense vacuolization in white matter, contrasting with very discrete infiltrates and degenerative changes in B2-/- mice after EAE induction.
Gene_expression (induction) of EAE in white matter associated with multiple sclerosis, inflammatory response and spinal cord
6) Confidence 0.23 Published 2008 Journal J Neuroinflammation Section Body Doc Link PMC2596102 Disease Relevance 0.93 Pain Relevance 0.35
In order to assess the involvement of kinin receptors in the cerebral chemokine release after EAE induction, brain tissues from WT and B2-/- were examined.
Gene_expression (induction) of EAE in brain associated with chemokine and multiple sclerosis
7) Confidence 0.23 Published 2008 Journal J Neuroinflammation Section Body Doc Link PMC2596102 Disease Relevance 1.11 Pain Relevance 0.27
There was no difference in cerebral CCL3 expression in WT mice before or after EAE induction (Figure 4C).
Gene_expression (induction) of EAE associated with multiple sclerosis
8) Confidence 0.23 Published 2008 Journal J Neuroinflammation Section Body Doc Link PMC2596102 Disease Relevance 1.23 Pain Relevance 0.32
expression after EAE induction.
Gene_expression (expression) of EAE associated with multiple sclerosis
9) Confidence 0.21 Published 2008 Journal J Neuroinflammation Section Body Doc Link PMC2596102 Disease Relevance 1.01 Pain Relevance 0.36
Our results suggest that PPNK accelerates the generation of autoimmune IFNgamma-producing T cells and MOG(35-55)-induced EAE.
Gene_expression (generation) of EAE in T cells associated with multiple sclerosis
10) Confidence 0.15 Published 2006 Journal J. Neuroimmunol. Section Abstract Doc Link 16904193 Disease Relevance 0.75 Pain Relevance 0
Gf enhancement of CVO differentiates EAE from control animals
Gene_expression (differentiates) of EAE associated with multiple sclerosis
11) Confidence 0.13 Published 2010 Journal J Neuroinflammation Section Body Doc Link PMC2978145 Disease Relevance 0.80 Pain Relevance 0.03
For a quantitative analysis of differences between EAE animals and naïve mice, we calculated the mean signal intensity ratio 24 h after Gf application in the CVO within these two groups (figure 5).
Gene_expression (animals) of EAE associated with multiple sclerosis
12) Confidence 0.13 Published 2010 Journal J Neuroinflammation Section Body Doc Link PMC2978145 Disease Relevance 0.78 Pain Relevance 0.21
In summary, endogenous androgens are protective in EAE in some strains but not others.
Gene_expression (protective) of EAE associated with multiple sclerosis and sprains and strains
13) Confidence 0.12 Published 2011 Journal Biol Sex Differ Section Body Doc Link PMC3022636 Disease Relevance 0.80 Pain Relevance 0.14
in developmentally normal mice was both necessary and sufficient for the oestrogen mediated protection in EAE remained unknown.
Gene_expression (protection) of EAE associated with multiple sclerosis
14) Confidence 0.12 Published 2011 Journal Biol Sex Differ Section Body Doc Link PMC3022636 Disease Relevance 0.43 Pain Relevance 0.10
This increased susceptibility in females compared to males is also present in animal models of autoimmune diseases such as spontaneous SLE in (NZBxNZW)F1 and NZM.2328 mice, experimental autoimmune encephalomyelitis (EAE) in SJL mice, thyroiditis, Sjogren's syndrome in MRL/Mp-lpr/lpr mice and diabetes in non-obese diabetic mice.
Gene_expression (syndrome) of encephalomyelitis associated with thyroiditis, multiple sclerosis, autoimmune disease, diabetes mellitus, syndrome, obesity and systemic lupus erythematosus
15) Confidence 0.12 Published 2011 Journal Biol Sex Differ Section Abstract Doc Link PMC3022636 Disease Relevance 1.92 Pain Relevance 0.13
While there is no perfect animal model of MS, experimental autoimmune encephalomyelitis (EAE) is the most widely used animal model for studying the pathogenesis of MS.
Gene_expression (is) of EAE associated with multiple sclerosis
16) Confidence 0.12 Published 2011 Journal Biol Sex Differ Section Body Doc Link PMC3022636 Disease Relevance 1.50 Pain Relevance 0.47
While there is no perfect animal model of MS, experimental autoimmune encephalomyelitis (EAE) is the most widely used animal model for studying the pathogenesis of MS.
Gene_expression (is) of encephalomyelitis associated with multiple sclerosis
17) Confidence 0.12 Published 2011 Journal Biol Sex Differ Section Body Doc Link PMC3022636 Disease Relevance 1.51 Pain Relevance 0.48
This increased susceptibility in females compared to males is also present in animal models of autoimmune diseases such as spontaneous SLE in (NZBxNZW)F1 and NZM.2328 mice, experimental autoimmune encephalomyelitis (EAE) in SJL mice, thyroiditis, Sjogren's syndrome in MRL/Mp-lpr/lpr mice and diabetes in non-obese diabetic mice.
Gene_expression (syndrome) of EAE associated with thyroiditis, multiple sclerosis, autoimmune disease, diabetes mellitus, syndrome, obesity and systemic lupus erythematosus
18) Confidence 0.12 Published 2011 Journal Biol Sex Differ Section Abstract Doc Link PMC3022636 Disease Relevance 1.91 Pain Relevance 0.13
Thus, while it is clear that high doses of oestradiol are protective in EAE, it has not yet been clearly established whether low doses of oestradiol are protective.
Gene_expression (protective) of EAE associated with multiple sclerosis
19) Confidence 0.12 Published 2011 Journal Biol Sex Differ Section Body Doc Link PMC3022636 Disease Relevance 1.23 Pain Relevance 0.12
Microglial MT-MMP expression in EAE
Gene_expression (expression) of EAE associated with multiple sclerosis
20) Confidence 0.12 Published 2007 Journal J Neuroinflammation Section Body Doc Link PMC2075488 Disease Relevance 0.99 Pain Relevance 0.20

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